血管内皮细胞凋亡是导致血管稳态失衡和重构的重要因素，因此，发现抑制血管内皮细胞凋亡的新因子及通路对控制血管稳态和重构至关重要。在预实验中，我们发现了一种抑制血管内皮细胞凋亡新长非编码RNA—AF007131，但是,其作用机制尚未搞清。生物信息学分析表明，它与miRNA-4707-5p和miRNA-4767有很强的结合能力，其靶基因分别是凋亡抑制因子API5和BCL2L12；过表达或敲低AF007131分别明显下调或上调这两个miRNAs，并上调或下调两者的靶基因，同时还能正调控其临近基因BCL2L10。因此，提出科学假设：AF007131一方面通过与miRNA结合进而上调其靶基因API5和BCL2L12；另一方面，通过改变BCL2L10其上的表观遗传修饰进而正调控BCL2L10，从而抑制细胞凋亡。我们拟利用培养的内皮细胞和ApoE-/-小鼠模型，证明该假设,为防治动脉硬化提供新靶点和线索。

It has been well accepted that vascular endothelium is critically involved in the maintenance of vascular homeostasis in health. Therefore, it is very important to discover the new apoptosis inhibitor or pathway in vascular endothelial cells for vascular homeostasis and remodeling. In our previous study, we found a new long noncoding RNA—AF007131 that inhibited vascular endothelial cell (VEC) apoptosis, but its action mechanism is unknown. By using bioinformatics programs, we known that the new long noncoding RNA may interact with miRNA-4707-5p and miRNA-4767 more strongly, and these two miRNAs may target anti-apoptosis factors API5(Apoptosis inhibitor-5）and BCL2L12 (Bcl2-Like 12，Bcl2L12) respectively. In our experiments, we demonstrated that overexpression of AF007131 down regulated miRNA-4707-5p and miRNA-4767, and positively regulated API5, BCL2L12 and its neighbor gene-BCL2L10; whereas, knockdown of AF007131 up regulated miRNA-4707-5p and miRNA-4767, and down regulated API5, BCL2L12 and its neighbor gene-BCL2L10 by using Quantitative real-time PCR. Based on these results and the latest literatures, we raise a hypothesis that, on the one hand, AF007131, which may interact with miRNA-4707-5p and miRNA-4767, up regulate API5 and BCL2L12 and then inhibit apoptosis; on the other hand, AF007131 may positively regulate BCL2L10 by epigenetic modification, further inhibit apoptosis. We will demonstrate our hypothesis by using binding site mutation, RNA interference, gene overexpression and luciferase reporter system, RNA pull-down，ChIP, RNA ChIP and other molecular/cell biological methods. By this study, we will provide new evidence for explaining the mechanism of this long noncoding RNA in control of vascular endothelial cell apoptosis, and discover new targets for prevention of vascular diseases.